肝细胞癌与缺氧:综述

Mohamed Elborei
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引用次数: 0

摘要

肝脏是我们体内最大的腺体,它在身体中有许多功能,但像身体的任何其他器官一样,它容易患上不同的疾病,但其中最危险的是肝细胞癌。肝细胞癌是胎儿期的,它的存活率很低,而且对大多数已知的治疗方法都有抗药性,这就是为什么总是需要新的治疗方式。它有不同的病因、不同的分期方法、不同的肝癌发生机制和不同的治疗方式,如肝切除、肝移植和索拉非尼。肿瘤缺氧是肝细胞癌和其他实体肿瘤的共同特征,它是由快速扩张的癌细胞缺乏血液供应引起的。肿瘤缺氧是一个不利的预后因素,因为它增强了肿瘤的侵袭性和对治疗的抵抗力,这就是为什么减少肿瘤缺氧对癌症患者有很多治疗益处。耐药、转移、血管生成、代谢移位、放疗抵抗、肿瘤总体侵袭性及预后不良均由缺氧诱导因子1引起,缺氧诱导因子1引起耐药、转移、血管生成、代谢移位、放疗抵抗、肿瘤总体侵袭性及预后不良。人们对肿瘤缺氧的研究非常活跃,试图发现新的药物和方法来纠正肿瘤缺氧,如缺氧激活的前药、高压氧、纳米颗粒、口服氧治疗,最后是缺氧诱导因子抑制剂如苯并吡喃、1,2,3-三唑、甘油、伏立诺他等。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hepatocellular Carcinoma & Hypoxia: A Review
Liver is the largest gland inside our body, and it is accounted for many functions in the body but like any other organ in the body it is prone to different disease but the most dangerous one of them is hepatocellular carcinoma. Hepatocellular carcinoma is fetal, and it is having low survival rate and it is resistant to the most of the know therapy that’s why there is always a need for new treatment modalities. It has different causative agents, different staging methods, different mechanism for hepatocarcinogenesis and different treatment modalities like liver resection, liver transplantation and sorafenib. Tumor hypoxia is a common feature of hepatocellular carcinoma and other solid tumours, and it results from a lack of blood supply to the rapidly expanding cancer cells. Tumor hypoxia is an unfavourable prognosis factor since it enhances the tumor's aggressiveness and resistance to treatment, which is why reducing tumour hypoxia has a lot of therapeutic benefits for cancer patients. Drug resistance, metastasis, angiogenesis, metabolic shifting, radiotherapy resistance, and overall tumour aggressiveness and poor prognosis are all caused by hypoxia inducible factor 1, which causes drug resistance, metastasis, angiogenesis, metabolic shifting, radiotherapy resistance, and overall tumour aggressiveness and poor prognosis. There is keen research working on the tumor hypoxia and trying to discover new drugs and approaches to correct the tumor hypoxia like prodrugs activated by hypoxia, hyperbaric oxygen, nanoparticles, oral oxygen therapy and finally hypoxia inducible factors inhibitors like for example benzopyranyl 1,2,3-triazole, glyceollins and vorinostat.
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